What is Graves’ Disease?

Graves' disease (GD) is an autoimmune thyroid disorder that primarily affects the thyroid gland, causing hyperthyroidism. It may also affect the eyes, causing Graves' ophthalmopathy (thyroid eye disease or TED); the skeletal muscles causing myopathy or muscle weakness; and the skin, causing pretibial myxedema and acropachy.

There are many GD variants or subtypes, and each individual case of GD is unique. Graves' disease is caused by stimulating TSH receptor antibodies, which are also known as thyroid stimulating immunoglobulins or TSI. These antibodies activate receptors on the surface of thyroid cells, ordering thyroid cells to produce more thyroid hormone. Like a key opening a lock, these antibodies cause a sustained increase in thyroid hormone levels.

Graves' disease primarily targets women between the ages of 30-50. However, it also affects men, and it can affect individuals of any age. GD can also affect muscle, causing muscle weakness, and it can affect heart muscle.

Patients with pretibial myxedema (PTM) may rarely develop a soft tissue disorder known as acropachy that primarily affects the fingers and toes. GD patients may also exhibit symptoms of clubbing which is different than acropachy.

As mentioned, the stimulating thyrotropin (or TSH) receptor antibodies seen in Graves' disease are also called thyroid stimulating immunoglobulins (TSI). These antibodies are directly responsible for the hyperthyroidism of Graves' disease. Acting in place of TSH, they direct the thyroid gland to keep producing and secreting excess thyroid hormone.

TSH is a pituitary hormone which regulates thyroid hormone levels in the blood. The concentration of TSH present in the blood is generally a good indicator of thyroid status, and levels of TSH are often used to diagnose thyroid disorders.

When thyroid hormone levels in the blood are low, the hypothalamus orders the pituitary to secrete more TSH and TSH levels are high. When thyroid hormone levels are elevated, the hypothalamus halts TSH release. Thus, in hyperthyroidism, levels of TSH are low, frequently lower than the detection level (usually <0.01 IU/L).

Thyroid hormones include thyroxine (T4)and triiodothyronine (T3). Normally, the thyroid primarily produces T4 along with a small amount of T3. T3, which is 10 times more active than T4, is mainly produced in the body by conversion (or losing one iodine molecule) from T4. Thyroid hormone is 65% iodine.

T4 has 4 iodine atoms, whereas T3 has 3 iodine atoms. However, in GD the thyroid gland produces more T3 relative to T4 than usual. This results in a condition known as T3 toxicosis. Despite it's ominous sound, T3 toxicosis is a good indicator of a favorable response to ant-thyroid drug therapy.

Who Gets Graves' Disease?

Graves' disease affects women 7 times more often than men. The peak age for GD is 20-40 years although young children and the elderly are also affected. Symptoms of GD in males are often more severe, and men are more likely to develop muscle disorders. Males are seldom diagnosed with GD until their symptoms are severe.

The Role of Genetic Factors

The true prevalence of GD is unknown, but it has been estimated to be slightly less than 1% of the U.S. population. In additon, as many as 3% to 4% of the population is thought to have subclincial Graves' disease, a condition in which the patient has no symptoms although lab tests paint a picture of hyperthyroidism.

Fifth Chakra Influences in GD

The fifth chakra is the throat chakra. It is related to our ability to speak out and voice our truth. If there is a blockage in the throat area, it may be due to holding back or not being comfortable enough in the world (third chakra influence) in order to express one’s ideas and feelings. Or one may feel powerless and feel the necessity of keeping secrets. However, when this center is open, individuals freely speak out and express their deepest ideas and feelings.

Iodine can trigger GD in susceptible individuals

A new model for the study of the role of iodine in inducing thyroid autoimmunity has become available in the form of the nonobese diabetic (NOD)-H2h4 mouse. This animal develops autoimmune thyroiditis spontaneously but in relatively low prevalence. However, if iodine is added to the drinking water, the prevalence and severity of the thyroid lesions increase markedly. ♦